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Clinical data
AHFS/Drugs.comMicromedex Detailed Consumer Information
ATC code
Pharmacokinetic data
Protein binding97%
  • (RS)-2-chloro-1-(difluoromethoxy)-1,1,2-trifluoroethane
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.034.126 Edit this at Wikidata
Chemical and physical data
Molar mass184.49 g·mol−1
3D model (JSmol)
  • FC(Cl)C(F)(F)OC(F)F
  • InChI=1S/C3H2ClF5O/c4-1(5)3(8,9)10-2(6)7/h1-2H checkY

Enflurane (2-chloro-1,1,2,-trifluoroethyl-difluoromethyl ether) is a halogenated ether. Developed by Ross Terrell in 1963, it was first used clinically in 1966. It was increasingly used for inhalational anesthesia during the 1970s and 1980s[1] but is no longer in common use.[2]

Enflurane is a structural isomer of isoflurane. It vaporizes readily, but is a liquid at room temperature.

Physical properties

Property Value
Boiling point at 1 atm 56.5 °C
MAC 1.68
Vapor pressure at 20 °C 22.9 kPa (172 mm Hg)
Blood:gas partition coefficient 1.9
Oil:gas partition coefficient 98

Side effects

Clinically, enflurane produces a dose-related depression of myocardial contractility with an associated decrease in myocardial oxygen consumption. Between 2% and 5% of the inhaled dose is oxidised in the liver, producing fluoride ions and difluoromethoxy-difluoroacetic acid. This is significantly higher than the metabolism of its structural isomer isoflurane.

Enflurane also lowers the threshold for seizures, and should especially not be used on people with epilepsy.[3] Like all potent inhalation anaesthetic agents it is a known trigger of malignant hyperthermia.

Like the other potent inhalation agents it relaxes the uterus in pregnant women which is associated with more blood loss at delivery or other procedures on the gravid uterus.

The obsolete (as an anaesthetic) agent methoxyflurane had a nephrotoxic effect and caused acute kidney injury, usually attributed to the liberation of fluoride ions from its metabolism. Enflurane is similarly metabolised but the liberation of fluoride results in a lower plasma level and enflurane related kidney failure seemed unusual if seen at all.[4]


The exact mechanism of the action of general anaesthetics has not been delineated.[5] Enflurane acts as a positive allosteric modulator of the GABAA,[6][7][8][9] glycine, and 5-HT3 receptors,[10][11] and as a negative allosteric modulator of the AMPA, kainate, and NMDA receptors,[11][12][13] as well as of nicotinic acetylcholine receptors.[10]

Occupational safety

The U.S. National Institute for Occupational Safety and Health (NIOSH) has set a recommended exposure limit (REL) for exposure to waste anaesthetic gas of 2 ppm (15.1 mg/m3) over a 60-minute period. Symptoms of occupational exposure to enflurane include eye irritation, central nervous system depression, analgesia, anesthesia, convulsions, and respiratory depression.[14]


  1. ^ Niedermeyer, Ernst; Silva, F. H. Lopes da (2005). Electroencephalography: Basic Principles, Clinical Applications, and Related Fields. Lippincott Williams & Wilkins. p. 1156. ISBN 978-0-7817-5126-1.
  2. ^ Pharmacology and Physiology for Anesthesia. 2013. doi:10.1016/C2009-0-41712-4. ISBN 9781437716795.
  3. ^ Khankhanian, Pouya; Himmelstein, Daniel (April 2004). "Enflurane has established ictogenic properties?". Thinklab. doi:10.15363/thinklab.d224. Retrieved October 17, 2016.
  4. ^ By G. Edward Morgan, Maged S. Mikhail, Michael J. Murray, C. Philip Larson; Clinical Anaesthesiology third edition,142.
  5. ^ "How does anesthesia work?".
  6. ^ M. Wakamori, Y. Ikemoto & N. Akaike (1991). "Effects of two volatile anesthetics and a volatile convulsant on the excitatory and inhibitory amino acid responses in dissociated CNS neurons of the rat". Journal of Neurophysiology. 66 (6): 2014–2021. doi:10.1152/jn.1991.66.6.2014. PMID 1667416.
  7. ^ M. V. Jones, P. A. Brooks & N. L. Harrison (1992). "Enhancement of gamma-aminobutyric acid-activated Cl- currents in cultured rat hippocampal neurones by three volatile anaesthetics". The Journal of Physiology. 449: 279–293. doi:10.1113/jphysiol.1992.sp019086. PMC 1176079. PMID 1326046.
  8. ^ M. D. Krasowski & N. L. Harrison (2000). "The actions of ether, alcohol and alkane general anaesthetics on GABAA and glycine receptors and the effects of TM2 and TM3 mutations". British Journal of Pharmacology. 129 (4): 731–743. doi:10.1038/sj.bjp.0703087. PMC 1571881. PMID 10683198.
  9. ^ L. H. Lin, L. L. Chen, J. A. Zirrolli & R. A. Harris (1992). "General anesthetics potentiate gamma-aminobutyric acid actions on gamma-aminobutyric acidA receptors expressed by Xenopus oocytes: lack of involvement of intracellular calcium". The Journal of Pharmacology and Experimental Therapeutics. 263 (2): 569–578. PMID 1331405.CS1 maint: multiple names: authors list (link)
  10. ^ a b Elaine K. Perry; Heather Ashton; Allan H. Young (2002). Neurochemistry of Consciousness: Neurotransmitters in Mind. John Benjamins Publishing. pp. 154–. ISBN 978-1-58811-124-1.
  11. ^ a b Charles J. Cote; Jerrold Lerman; Brian J. Anderson (2013). A Practice of Anesthesia for Infants and Children: Expert Consult - Online and Print. Elsevier Health Sciences. pp. 499–. ISBN 978-1-4377-2792-0.
  12. ^ Paul Barash; Bruce F. Cullen; Robert K. Stoelting; Michael Cahalan; Christine M. Stock; Rafael Ortega (7 February 2013). Clinical Anesthesia, 7e: Print + Ebook with Multimedia. Lippincott Williams & Wilkins. pp. 116–. ISBN 978-1-4698-3027-8.
  13. ^ Lin LH, Chen LL, Harris RA (1993). "Enflurane inhibits NMDA, AMPA, and kainate-induced currents in Xenopus oocytes expressing mouse and human brain mRNA". FASEB J. 7 (5): 479–85. doi:10.1096/fasebj.7.5.7681790. PMID 7681790. S2CID 1050582.
  14. ^ "CDC - NIOSH Pocket Guide to Chemical Hazards - Enflurane". www.cdc.gov. Retrieved 2015-10-01.